Physiology publishes focused review articles written by leaders in their fields. These articles are peer reviewed and highlight major cutting-edge advances in different fields of physiology. The Editorial Board for Physiology comprises leaders in the broad field of physiology and meets annually to discuss and recommend leading-edge topics for review articles as well as the scientists who could best write these review articles.
Cortactin, an actin filament-binding protein and target of multiple kinases, has emerged as a central element connecting signaling pathways with cytoskeleton restructuring. It is involved in a perplexingly diverse array of cellular processes, including cell motility, invasiveness, synaptogenesis, endocytosis, intercellular contact assembly, and host-pathogen interactions, where the common denominator appears to be a role in the coordination of membrane dynamics with cytoskeletal remodeling. Although in recent years our knowledge about cortactin has increased exponentially, the exact mechanisms underlying its fundamental roles remain to be defined.
Sufficient uteroplacental blood flow is essential for normal pregnancy outcome and is accomplished by the coordinated growth and remodeling of the entire uterine circulation, as well as the creation of a new fetal vascular organ: the placenta. The process of remodeling involves a number of cellular processes, including hyperplasia and hypertrophy, rearrangement of existing elements, and changes in extracellular matrix. In this review, we provide information on uterine blood flow increases during pregnancy, the influence of placentation type on the distribution of uterine vascular resistance, consideration of the patterns, nature, and extent of maternal uterine vascular remodeling during pregnancy, and what is known about the underlying cellular mechanisms.
Tight junctions form selective barriers that regulate paracellular transport across epithelia. A large family of tetraspanning cell-cell adhesion proteins called claudins create the barrier and regulate electrical resistance, size, and ionic charge selectivity. Study of inherited human claudin diseases and the outcome of the genetic manupulation of claudins in mice, Drosophila, and Caenorhabditis elegans are furthering our understanding of paracellular physiology.
Sirtuins comprise a family of enzymes implicated in the determination of organismal life span in yeast and the nematode. The mammalian sirtuin SIRT1 has been shown to deacetylate several proteins in an NAD+-dependent manner. SIRT1 substrates are involved in the regulation of apoptosis/cell survival, endocrine signaling, differentiation, chromatin remodeling, and transcription. Thus SIRT1 provides a molecular link between nutrient availability and adaptive transcriptional responses. This review presents current evidence as to how SIRT1 functions are relevant to changes in tissue physiology that occur with ageing and its implications for future pharmacological intervention to alleviate such degenerative processes.
Sílvia Graciela Ruginsk, André S. Mecawi, Melina P. da Silva, Wagner Luis Reis, Ricardo Coletti, Juliana Bezerra Medeiros de Lima, Lucila Leico Kagohara Elias, José Antunes‐Rodrigues
Nitric oxide (NO), carbon monoxide (CO), and hydrogen sulfide (H2S) are gaseous molecules produced by the brain. Within the hypothalamus, gaseous molecules have been highlighted as autocrine and paracrine factors regulating endocrine function. Therefore, in the present review, we briefly discuss the main findings linking NO, CO, and H2S to the control of body fluid homeostasis at the hypothalamic level, with particular emphasis on the regulation of neurohypophyseal system output.
Biliverdin reductase (BVR) functions in cell signaling through three distinct tracks: a dual-specificity kinase that functions in the insulin receptor/MAPK pathways ( 25 , 29 , 51 ); a bzip-type transcription factor for ATF-2/CREB and HO-1 regulation ( 1 , 25 ); and a reductase that catalyzes the conversion of biliverdin to bilirubin ( 27 ). These, together with the protein’s primary and secondary features, intimately link BVR to the entire spectrum of cell-signaling cascades.
The ability to sense and respond to changes in oxygenation represents a fundamental property of all metazoan cells. The discovery of the transcription factor HIF-1 has led to the identification of protein hydroxylation as a mechanism by which changes in Po2 are transduced to effect changes in gene expression.
Muscle performance is influenced by turnover of contractile proteins. Production of new myofibrils and degradation of existing proteins is a delicate balance, which, depending on the condition, can promote muscle growth or loss. Protein synthesis and protein degradation are coordinately regulated by pathways that are influenced by mechanical stress, physical activity, availability of nutrients, and growth factors. Understanding the signaling that regulates muscle mass may provide potential therapeutic targets for the prevention and treatment of muscle wasting in metabolic and neuromuscular diseases.
Signaling through mammalian target of rapamycin (mTOR) is activated by amino acids, insulin, and growth factors, and impaired by nutrient or energy deficiency. mTOR plays key roles in cell physiology. mTOR regulates numerous components involved in protein synthesis, including initiation and elongation factors, and the biogenesis of ribosomes themselves.
Rat muscle studies suggest competition between free fatty acids (FFA) and glucose for oxidation, resulting in glucose-6-phosphate accumulation. However, FFA decrease glucose-6-phosphate in human skeletal muscle, indicating direct inhibition of glucose transport/phosphorylation. This mechanism could redirect glucose from muscle to brain during fasting and explain the insulin resistance associated with high-lipid diets and obesity.
Chỉ số ảnh hưởng
Total publication
1
Total citation
155
Avg. Citation
155
Impact Factor
0
H-index
1
H-index (5 years)
1
i10
1
i10-index (5 years)
0
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